Hyponatremia occurs as a result of a positive balance of EFW, either through the administration, and/or the inability to excrete EFW. Antidiuretic hormone (ADH) increases the permeability of the distal renal tubule and collecting duct, resulting in renal concentration of EFW and inappropriately high urinary sodium concentration. Advocates of isotonic fluids therefore argue that maintaining plasma tonicity supercedes the need to maintain nutritional sodium intake during acute illness, at a time when the non-osmotic ADH secretion and impaired EFW excretion predominate(5). Those who argue against isotonic fluids use suggest that hyponatremia is a result of the misuse and over-administration of appropriate hypotonic solutions(6). The traditional calculation for maintenance fluid requirements in hospitalized children has been criticized for overestimating energy expenditure and subsequently free-water requirements, and the total fluid requirements during acute illness or following surgery may approximate only half of that suggested by traditional recommendations (50-60 mL/kg/day)(5). Hence, in susceptible, euvolemic patients, both isotonic or hypotonic maintenance solutions may both result in a net increase in serum sodium if the "desalination" induced by ADH is negated with fluid restriction. It is important to emphasize however, in volume depleted patients, elevated ADH secretion and increased urinary tonicity persists until adequate volume expansion is achieved(7). The significantly lower total fluid intake in hyponatremic patients in comparison to controls may be suggestive of this phenomenon in the present study(3).

Where no relationship is observed between EFW balance and the fall in serum sodium, a translocational hyponatremia with increased osmolar gap, termed the "sick cell syndrome", has been hypothesized in the development early hyponatremia in critically ill adults, while a dilutional mechanism may be more responsible for ongoing hypo-natremia(8). It is yet unclear what role this phenomenon plays in the etiology of hyponatremia in children. If hyponatremia was purely a problem of dilution, then all hypotonic solutions should be abandoned. The study by Singhi, et al.(3) provides further evidence of multifactorial mechanisms unique to each patient, and while a fall in serum sodium was not consistently attributable to a positive EFW balance, the risks of significant hyponatremia during hypotonic fluid administration were substantial (36.8% of patients).

There is, therefore, no simple formula or single solution of choice that will guarantee tonicity balance and minimize electrolyte disturbances in children other than vigilance with monitoring and "dose adjusting" our prescriptions according to the patient’s response. It is often difficult to assess a child’s extracellular volume status, and knowing the serum electrolytes at presentation may not reliably predict how these will evolve with an empiric and generic fluid prescription, particularly in complex and critically ill children. Our current maintenance fluid prescription practice in children is challenging in light of the disturbing paucity of evidence. Until more prospective trials are undertaken, the safest solution is to tailor fluid prescriptions to the individual patient, needs over time, and focus on the inherent properties of the patient’s physiology, rather than the inherent properties of the fluid being used.

1. Moritz ML, Ayus JC. Hospital-acquired hyponatremia: why are there still deaths? Pediatrics 2004;113: 1395-1396.

2. Holliday MA. Isotonic saline expands extracellular fluid and is inappropriate for maintenance therapy. Pediatrics 2005; 115: 193-194.

3. Singhi S, Jayashree M. Free water excess is not the main cause for hyponatremia in critically ill children receiving conventional maintenance fluids. Indian Pediatr 2009; 46: 577-583.

4. Hoorn EJ, Geary D, Robb M, Halperin ML, Bohn D. Acute hyponatremia related to intravenous fluid administration in hospitalized children: an observational study. Pediatrics 2004; 113: 1279-1284.

5. Taylor D, Durward A. Pouring salt on troubled waters. Arch Dis Child 2004; 89: 411-414.

6. Holliday MA, Friedman A, Segar ME, Chesney R, Finberg L. Acute hospital induced hyponatremia in children: A physiologic approach. J Pediatr 2004; 145: 584-587.

7. Powell KR, Sugarmann LI, Eskanazi AE. Normalisation of plasma arginine vasopressin concentrations when children with meningitis are given maintenance plus replacement fluid therapy. J Pediatr 1990;117: 515-522.